Epidermal barrier reaction to an in vitro psoriatic microenvironment

Elena Donetti, Laura Cornaghi, Francesca Arnaboldi, Federica Ricceri, Leonardo Pescitelli, Martina Maiocchi, Francesco Carriero, Franz Baruffaldi Preis, Francesca Prignano

Research output: Contribution to journalArticlepeer-review


Keratinocytes (KCs) and Langerhans cells (LCs) contribute to create the epidermal barrier. To form a functional epidermis, KCs express filaggrin and Toll-like Receptors (TLRs). LCs are the first line of epidermal defence and can be activated by interleukin (IL)-17 and Tumor Necrosis Factor (TNF)-alpha. In psoriasis, an alteration of TLR expression, a defective expression of filaggrin, and LC activation occur. In organotypic cultures of human skin we investigated the interplay between IL-17 and TNF-alpha on i) expression of filaggrin, TLR2, 7 and 9, and Nuclear Factor (NF)-kB localization by immunofluorescence and ii) LC ultrastructural features by transmission electron microscopy. Normal human skin was obtained after aesthetic surgery (n=7), overnight incubated in a Transwell system, and exposed to TNF-alpha and/or IL-17 for 24 (T24), 48 (T48), and 72 (T72) hours. Cytokines always influenced the expression of filaggrin. TNF-alpha alone activated LCs only starting from T48. TLR2 and TLR7 expressions were affected at T24 by IL-17 and the combination of cytokines, but not by TNF-alpha. TLR9-positive cells were detectable in the granular layer after cytokine exposure. A nuclear localization of NF-kB was always observed after cytokine incubation. In conclusion, each cytokine possess an intrinsic activity on the different components of the epidermal barrier.

Original languageEnglish
Pages (from-to)180-188
Number of pages9
JournalExperimental Cell Research
Issue number2
Publication statusPublished - Nov 15 2017
Externally publishedYes


  • Immunofluorescence
  • Innate immunity
  • Langerhans cells
  • Nuclear factor kappa B
  • TLRs
  • Transmission electron microscopy

ASJC Scopus subject areas

  • Cell Biology


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